NEW PROSTATE CANCER INFOLINK: Prostate cancer is linked to gene variations we inherit, but there are other factors involved as well, writes Mike Scott. READ MORE>

It is all too easy to want to believe that prostate cancer (and other forms of cancer) might be like one of the truly heritable diseases that are utterly dependent on one’s genetics, such as sickle cell anemia or Huntington’s disease.

Unfortunately, it just isn’t going to be that simple.

The development of prostate cancer in any specific individual is most probably a multi-stage process.

It may well be linked to the genes you are born with, but it is also quite certainly linked to other things that happen as you age.

As yet, we have minimal understanding of what those “other things” really are.

US PROSTATE CANCER FOUNDATION: The primary cause of prostate cancer could be the fusion of two genes and the subsequent abnormal prostate cell growth that results when receptors for the hormone androgen get blocked, a new study reveals. READ MORE>

URO TODAY: Researchers have investigated associations between 29 single nucleotide polymorphisms (SNP) and biochemical recurrence, castration-resistant metastasis, and prostate cancer-specific survival, and found the SNPs are a clue to outcomes. READ MORE>

When the damage is not repaired, the outcome may be cancer – or, if cell death or senescence (aging) occurs, protection from cancer – but the trade-off is acceleration of the aging process.

The development of cancer and the process of aging can be delayed by reducing the load of DNA damage — by avoiding or limiting exposure to exogenous genotoxins and by suppressing metabolism — thereby producing fewer reactive species.

However, DNA damage, like caloric (calories) restriction, can also elicit a protective survival response that promotes longevity and healthy aging.

Recently, the use of (immuno-suppressant drug) sirolimus in mice was found to extend their life span and delay the development of conditions associated with aging, including cancer. Sirolimus is one of presumably many compounds that may elicit the survival response.

The frequent derailment of DNA damage-response systems in tumours presents another possible route by which new treatments can act selectively on the tumor.